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Updated: Mar 27, 2026

Single Port Donor Nephrectomy
Published on: March 12, 2011
Cardiovascular Effects of Unilateral Nephrectomy in Living Kidney Donors
William E Moody1, Charles J Ferro1, Nicola C Edwards1
1From the Birmingham Cardio-Renal Group, Institute of Cardiovascular Science, Departments of Cardiology (W.E.M., N.C.E., C.D.C., E.L.S.L., R.J.T., R.P.S., J.N.T.) and Nephrology (C.J.F., P.C.), Queen Elizabeth Hospital Birmingham and University of Birmingham, Edgbaston, United Kingdom.
Insights
Living kidney donation leads to reduced kidney function (GFR), increasing cardiovascular risks. This study found donors developed higher left ventricular mass and impaired heart function, suggesting reduced GFR is a direct cardiovascular risk factor.
Area of Science:
- Nephrology
- Cardiology
- Biomedical Research
Background:
- A robust inverse association exists between glomerular filtration rate (GFR) and cardiovascular risk, but causality remains unproven.
- Emerging data suggest living kidney donation may increase cardiovascular mortality, yet mechanisms are unclear.
Purpose of the Study:
- To investigate if reduced GFR in living kidney donors is associated with adverse cardiovascular changes.
- To assess changes in left ventricular mass, function, and aortic stiffness post-donation.
Main Methods:
- A multicenter, parallel group, blinded end-point study comparing 124 living kidney donors and healthy controls.
- Primary outcome: change in left ventricular mass via MRI from baseline to 12 months.
- Secondary outcomes included aortic distensibility, cardiac function, and biomarkers.
Main Results:
- Donors experienced a significant decrease in GFR (-30±12 mL/min/1.73m²).
- Donors showed increased left ventricular mass (+7±10 g) and mass:volume ratio, with decreased aortic distensibility and global circumferential strain compared to controls.
- Donors had higher risks of detectable high-sensitivity troponin T and microalbuminuria; serum uric acid, PTH, FGF-23, and hs-CRP increased.
Conclusions:
- Reduced GFR in living kidney donors is linked to adverse cardiac remodeling and impaired function.
- These findings support considering reduced GFR as an independent causative cardiovascular risk factor.
Unlabelled:
There is a robust inverse graded association between glomerular filtration rate (GFR) and cardiovascular risk, but proof of causality is lacking. Emerging data suggest living kidney donation may be associated with increased cardiovascular mortality although the mechanisms are unclear. We hypothesized that the reduction in GFR in living kidney donors is associated with increased left ventricular mass, impaired left ventricular function, and increased aortic stiffness. This was a multicenter, parallel group, blinded end point study of living kidney donors and healthy controls (n=124), conducted from March 2011 to August 2014. The primary outcome was a change in left ventricular mass assessed by magnetic resonance imaging (baseline to 12 months). At 12 months, the decrease in isotopic GFR in donors was -30±12 mL/min/1.73m(2). In donors compared with controls, there were significant increases in left ventricular mass (+7±10 versus -3±8 g; P<0.001) and mass:volume ratio (+0.06±0.12 versus -0.01±0.09 g/mL; P<0.01), whereas aortic distensibility (-0.29±1.38 versus +0.28±0.79×10(-3) mm Hg(-1); P=0.03) and global circumferential strain decreased (-1.1±3.8 versus +0.4±2.4%; P=0.04). Donors had greater risks of developing detectable highly sensitive troponin T (odds ratio, 16.2 [95% confidence interval, 2.6-100.1]; P<0.01) and microalbuminuria (odds ratio, 3.8 [95% confidence interval, 1.1-12.8]; P=0.04). Serum uric acid, parathyroid hormone, fibroblast growth factor-23, and high-sensitivity C-reactive protein all increased significantly. There were no changes in ambulatory blood pressure. Change in GFR was independently associated with change in left ventricular mass (R(2)=0.28; P=0.01). These findings suggest that reduced GFR should be regarded as an independent causative cardiovascular risk factor.
Clinical Trial Registration:
URL: http://www.clinicaltrials.gov. Unique identifier: NCT01028703.
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